The proposed interrelated projects are designed to provide answers relating to the mechanism as well as prenatal diagnosis and treatment of various forms of surfactant damage which represents the basic underlying defect in HMD of newborn and in other pathologic conditions of the lung. A significant aspect of this program is to study the prenatal and postnatal responses of develping lung to the injurious effect of factors which may be of significance in the pathogenesis of HMD. Specific Aims: 1. To apply new criteria, already established in our laboratory for the characterization and quantitation of normal and altered surfactant fractions recovered from (a) the lung of infants with and without HMD, (b) the amniotic fluid obtained prior to premature delivery following normal and abnormal pregnancies and, (c) lungs of fetus and newborn animals following in utero distress induced by maternal administration of e. coli endotoxin. 2. To study the sequence of structural and biochemical events associated with depressed biosynthesis versus inactivation of surfactant components in developing lungs of fetus and newborn following endotoxin induced fetal distress. 3. To evaluate whether glucocorticosteroids, known to accelerate the appearance of inclusion bodies and surfactant in fetal lungs, prevents or modifies endotoxin induced fetal lung lesions and associated damage to the surfactant system.